Smooth muscle actin-expressing stromal fibroblasts in head and neck squamous cell carcinoma: increased expression of galectin-1 and induction of poor prognosis factors
Language English Country United States Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
22447203
DOI
10.1002/ijc.27550
Knihovny.cz E-resources
- MeSH
- Actins biosynthesis genetics metabolism MeSH
- Stromal Cells metabolism pathology MeSH
- Down-Regulation MeSH
- Galectin 1 biosynthesis genetics metabolism MeSH
- Galectin 3 genetics metabolism MeSH
- Transcription, Genetic MeSH
- Muscle, Smooth metabolism pathology MeSH
- Humans MeSH
- Myofibroblasts metabolism pathology MeSH
- Head and Neck Neoplasms genetics metabolism pathology MeSH
- NF-kappa B genetics metabolism MeSH
- Prognosis MeSH
- RNA Splicing MeSH
- Carcinoma, Squamous Cell genetics metabolism pathology MeSH
- Up-Regulation MeSH
- Check Tag
- Humans MeSH
- Male MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Actins MeSH
- Galectin 1 MeSH
- Galectin 3 MeSH
- NF-kappa B MeSH
Tumor stroma is an active part influencing the biological properties of malignancies via molecular cross-talk. Cancer-associated fibroblasts play a significant role in this interaction. These cells frequently express smooth muscle actin and can be classified as myofibroblasts. The adhesion/growth-regulatory lectin galectin-1 is an effector for their generation. In our study, we set the presence of smooth muscle actin-positive cancer-associated fibroblasts in relation to this endogenous lectin and an in vivo competitor (galectin-3). In squamous cell carcinomas of head and neck, upregulation of galectin-1 presence was highly significantly correlated to presence of smooth muscle actin-positive cancer-associated fibroblasts in the tumor (p = 4 × 10(-8)). To pinpoint further correlations on the molecular level, we applied microarray analyses to the transcription profiles of the corresponding tumors. Significant correlations of several transcripts were detected with the protein level of galectin-1 in the cancer-associated fibroblasts. These activated genes (MAP3K2, TRIM23, PTPLAD1, FUSIP1, SLC25A40 and SPIN1) are related to known squamous-cell-carcinoma poor-prognosis factors, NF-κB upregulation and splicing downregulation. These results provide new insights into the significance of presence of myofibroblasts in squamous cell carcinoma.
References provided by Crossref.org
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